The Human Visceral Fat Depot Has a Unique Inflammatory Profile

Abstract

Obesity can be considered as a low‐grade inflammatory condition, strongly linked to adverse metabolic outcomes. Obesity‐associated adipose tissue inflammation is characterized by infiltration of macrophages and increased cytokine and chemokine production. The distribution of adipose tissue impacts the outcomes of obesity, with the accumulation of fat in visceral adipose tissue (VAT) and deep subcutaneous adipose tissue (SAT), but not superficial SAT, being linked to insulin resistance. We hypothesized that the inflammatory gene expression in deep SAT and VAT is higher than in superficial SAT. A total of 17 apparently healthy women (BMI: 29.3±5.5 kg/m2) were included in the study. Body fat (dual‐energy X‐ray absorptiometry) and distribution (computed tomography) were measured, and insulin sensitivity, blood lipids, and blood pressure were determined. Inflammation‐related differences in gene expression (real‐time PCR) from VAT, superficial and deep SAT biopsies were analyzed using univariate and multivariate data analyses. Using multivariate discrimination analysis, VAT appeared as a distinct depot in adipose tissue inflammation, while the SAT depots had a similar pattern, with respect to gene expression. A significantly elevated (P < 0.01) expression of the CC chemokine receptor 2 (CCR2) and macrophage migration inhibitory factor (MIF) in VAT contributed strongly to the discrimination. In conclusion, the human adipose tissue depots have unique inflammatory patterns, with CCR2 and MIF distinguishing between VAT and the SAT depots.

Gene silencing in adipose tissue macrophages regulates whole-body metabolism in obese mice

“…1 and 2). This selective biodistribution profile of i.p.-injected GeRPs in obese mice is in keeping with the known high accumulation of macrophages in visceral AT compared with other adipose depots and metabolic tissues in obese rodents and humans (9,25,26). In previous studies using lean healthy animals, i.p.-injected GeRPs were internalized by macrophages that could be detected throughout the body (13,15).…”

Androgenic sex steroids contribute to metabolic risk beyond intra‐abdominal fat in overweight/obese black and white women

“…Thus, it is not surprising that VAT more so than SAT was positively associated with a constellation of metabolic variables characteristic of the metabolic syndrome and CVD risk. Although SAT does have some of the same metabolic effects as VAT, it is not as strongly correlated with proinflammatory, hyperinsulinemic markers (29,30). Of the metabolic variables examined, SAT had a significant relationship with SBP only.…”

Heterogeneity of adipose tissue in development and metabolic function

“…Yet, if this inflammatory response is not tightly controlled, or combined with other inflammatory stimuli such as adipocyte death, this results in a detrimental metabolic outcome. VAT exhibits a more proinflammatory cytokine expression profile compared with SAT in both humans and mice, including IL-6, interleukin 8 (IL-8), monocyte chemotactic protein1 (MCP-1), RANTES, macrophage inflammatory protein 1 alpha (MIP-1a) and plasminogen activator inhibitor 1 (PAI-1) (Alvehus et al, 2010;Kwok et al, 2016;Lee et al, 2013c), which is further enhanced in obese subjects (Ouchi et al, 2011) (Fig. 2).…”